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Pick up to three peptides to see how their mechanisms, studied uses and evidence levels differ. Rows where the entries disagree are marked with a blue edge.
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Comparison
MOTS-C
Mitochondrial & antioxidant
Evidence level
Anecdotal evidence
Approval status
Not approved
Mechanism of action
- 1.Activates AMPK, the cell's energy-sensing switch, in skeletal muscle.
- 2.Moves into the nucleus under metabolic stress and influences gene expression.
- 3.Improves insulin sensitivity and glucose uptake in animal studies.
- 4.Reproduces some effects of exercise in mice, including fat oxidation.
- 5.Human evidence is largely observational: circulating MOTS-C levels track with insulin sensitivity, but raising them by injection has not been shown to help.
Studied for
- Insulin resistance and type 2 diabetes (animal and observational human work)
- Obesity and metabolic syndrome
- Exercise physiology and ageing research
- Vascular and cardiac protection in animal models
Reported effects
- Improved glucose tolerance and insulin sensitivity in mice
- Reduced fat mass and higher energy expenditure in animal models
- Uncertain effects in people; only very small studies exist
Side effects
- Reported: headache, nausea, fatigue
- Injection-site reactions
- No systematic safety data exist
- Effects on heart rate and blood pressure are unknown
Research protocol
Research context only — there is no approved protocol and no established human dose. Published animal work used microgram-per-kilogram doses. The 200 microgram to 1 mg daily schedules and multi-week 'build-up' charts sold by vendors come from community use, not clinical research, and syringe units depend entirely on the concentration in the vial.
Research context only
Evidence justification
The mitochondrial biology is genuinely interesting, but there are no meaningful controlled human trials of administered MOTS-C; human evidence is limited to small observational correlations.